López Millán, BelénCostales, PaulaGutiérrez Agüera, FranciscoDíaz de la Guardia, RafaelRoca Ho, HeleiaVinyoles, MeritxellRubio Gayarre, AlbaSafi, RémiCastaño, JulioRomecín, Paola AlejandraRamirez Orellana, ManuelAnguita Mandly, EduardoJeremías, IrmelaZamora, LurdesRodríguez Manzaneque, Juan CarlosBueno, ClaraMorís, FranciscoMenéndez, Pablo2023-06-222023-06-2220222072-669410.3390/cancers14061593https://hdl.handle.net/20.500.14352/71621Patients with AML harboring constitutively active mutations in the FLT3 receptor generally have a poor prognosis (FLT3-ITDMUT). Despite the fact that several FLT3 inhibitors have been developed, clinical responses are commonly partial or not durable, highlighting the need for new molecules targeting FLT3-ITDMUT. Here, we tested EC-70124, a hybrid indolocarbazole analog from the same chemical space as midostaurin (a well-known FLT3 inhibitor). Our in vitro and in vivo experiments showed that EC-70124 exerts a robust and specific antileukemia activity against FLT3-ITDMUT AML cells while sparing healthy hematopoietic cells. Collectively, EC-70124 is a promising and safe agent for the treatment of this aggressive type of AML.engAtribución 3.0 Españajournal articlehttps://doi.org/10.3390/cancers14061593https://www.mdpi.com/2072-6694/14/6/1593/htmopen accessAMLEC-70124 multi-kinase inhibitorFLT3-ITD mutationFLT3 inhibitorAML preclinical modelOncología3201.01 Oncología